Gene Expression Analysis of Endometrium Reveals Progesterone Resistance and Candidate Susceptibility Genes in Women with Endometriosis

Burney, Richard O.; Talbi, Saïd; Hamilton, Amy E.; Vo, Kim Chi; Nyegaard, Mette; Nezhat, Camran; Lessey, Bruce A.; Giudice, Linda C.

doi:10.1210/en.2006-1692

Cited by 657 publications

(648 citation statements)

References 83 publications

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“…In addition, compelling molecular evidence has shown fundamental differences in the endometrium from women with endometriosis compared to endometrium from women without endometriosis. Endometrium from women with endometriosis seems to have decreased expression of integrin [16] and HOXA10 [17], alterations in apoptosis [18], and a gene expression profile consistent with progesterone resistance [19]. We did not evaluate molecular data in this study and the only measure of endometrial receptivity we studied, endometrial thickness, was similar in patients before and after surgery ( Table 2).…”

Section: Discussionmentioning

confidence: 95%

Embryo quality before and after surgical treatment of endometriosis in infertile patients

Shahine

Burney

Behr

et al. 2009

J Assist Reprod Genet

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Section: Discussionmentioning

confidence: 95%

Embryo quality before and after surgical treatment of endometriosis in infertile patients

Shahine

Burney

Behr

et al. 2009

J Assist Reprod Genet

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“…Of the hundreds of gene expression changes typically identified by microarray, relatively few are common to more than two studies [47,48]. Comparison of proteomic data with published gene expression data in similar cohorts of women [47,49,50] also have revealed an overall lack of correlation between the two, suggesting that posttranscriptional or translational regulation is an important feature in human biology.…”

Section: Discussionmentioning

confidence: 99%

Protein expression in human cumulus cells as an indicator of blastocyst formation and pregnancy success

Braga

Setti

Turco

et al. 2016

J Assist Reprod Genet

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Purpose The goal for the present study was to implement a technique for protein extraction and identification in human cumulus cells (CCs). Methods Forty samples of CCs were collected after ovum pick-up from patients undergoing intracytoplasmic sperm injection (ICSI). Samples were split into the blastocyst group (n = 10), including patients in which all embryos converted into blastocysts, and the non-blastocyst group (n = 10), including patients in which none of the embryos reached the blastocyst stage or the positive-pregnancy (n = 10) and negativepregnancy group (n = 10). Proteins were extracted and injected into a liquid chromatography system coupled to a mass spectrometer. The spectra were processed and used to search a database. Results There were 87 different proteins in samples from the blastocyst and non-blastocyst groups, in which 30 were exclusively expressed in the blastocyst group and 17 in the nonblastocyst group. Among the 72 proteins detected in the pregnancy groups, 19 were exclusively expressed in the positive, and 16 were exclusively expressed in the negative-pregnancy group. Conclusions CC proteomics may be useful for predicting pregnancy success and the identification of patients that should be included in extended embryo culture programs.

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“…many cancers including hormonally regulated ones such as breast and prostate (26). In other diseases of the endometrium that display abnormal proliferation and P 4 resistance such as in endometriosis, the regulation of MCMs by P 4 is also lost (47). P 4 represents a rare example in vivo of a well-characterized physiological negative regulator of cell division.…”

Section: Ishikawa Cell Proliferation Is Negatively Regulated By Klf15mentioning

confidence: 99%

KLF15 negatively regulates estrogen-induced epithelial cell proliferation by inhibition of DNA replication licensing

Ray

Pollard²

2012

Proc. Natl. Acad. Sci. U.S.A.

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In the epithelial compartment of the uterus, estradiol-17β (E 2 ) induces cell proliferation while progesterone (P 4 ) inhibits this response and causes differentiation of the cells. In this study, we identified the mechanism whereby E 2 and P 4 reciprocally regulate the expression of minichromosome maintenance (MCM)-2, a protein that is an essential component of the hexameric MCM-2 to 7 complex required for DNA synthesis initiation. We show in the uterine epithelium that Kruppel-like transcription (KLF) factors, KLF 4 and 15, are inversely expressed; most importantly, they bind to the Mcm2 promoter under the regulation of E 2 and P 4 E 2 , respectively. After P 4 E 2 exposure and in contrast to E 2 treated mice, the Mcm2 promoter displays increased histone 3 (H3) methylation and the recruitment of histone deacetylase 1 and 3 with the concomitant deacetylation of H3. This increased methylation and decreased acetylation is associated with an inhibition of RNA polymerase II binding, indicating an inactive Mcm2 promoter following P 4 E 2 treatment. Using transient transfection assays in the Ishikawa endometrial cell line, we demonstrate that Mcm2 promoter activity is hormonally stimulated by E 2 and that KLF15 inhibits this E 2 enhanced transcription. KLF15 expression also blocks Ishikawa cell proliferation through inhibition of MCM2 protein level. Importantly, in vivo expression of KLF15 in an estrogenized uterus mimics P 4 's action by inhibiting E 2 -induced uterine epithelial MCM-2 expression and DNA synthesis. KLF15 is therefore a downstream physiological mediator of progesterone's cell cycle inhibitory action in the uterine epithelium.endometrium | implantation | menstrual cycle | endometriosis E stradiol-17β (E 2 ) and progesterone (P 4 ) directs uterine preparation for pregnancy. These hormones synthesized cyclically in humans cause a sequential series of proliferative and differentiation events in the uterine stroma and epithelium that result in the epithelium being receptive to the blastocyst for attachment and subsequent implantation (1). Despite this close control of uterine cell proliferation, aberrant proliferative conditions of the human endometrium are common. For example, endometrial polyps and endometriosis are caused by inappropriate proliferation of the uterus, while unopposed estrogen stimulation is associated with menstrual irregularities and endometrial hyperplasia/adenocarcinoma (2). Endometrial cancer is the most common female genital tract malignancy and is responsible for 6% of cancer deaths of women in the United States and more worldwide (3). However, the molecular mechanisms underlying these pathologies are still obscure, as are the molecular mechanisms involved in normal hormonal regulation of cell proliferation in the endometrium, which is essential for successful pregnancy (4).The mouse uterus provides a unique in vivo model to study the regulation of epithelial cell proliferation as the physiological actions of E 2 and P 4 E 2 can be recapitulated in ovariectomized animals by treat...

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Gene Expression Analysis of Endometrium Reveals Progesterone Resistance and Candidate Susceptibility Genes in Women with Endometriosis

Cited by 657 publications

References 83 publications

Embryo quality before and after surgical treatment of endometriosis in infertile patients

Embryo quality before and after surgical treatment of endometriosis in infertile patients

Protein expression in human cumulus cells as an indicator of blastocyst formation and pregnancy success

KLF15 negatively regulates estrogen-induced epithelial cell proliferation by inhibition of DNA replication licensing

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